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Single-cell RNA-sequencing of bleomycin-injured young and old mice

ABSTRACT: Single-cell RNA-sequencing of bleomycin-injured young and old mice

PROVIDER: PRJNA663600 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12645805.fastq.gz	Fastqsanger.gz
	SRR12645710.fastq.gz	Fastqsanger.gz
	SRR12645810.fastq.gz	Fastqsanger.gz
	SRR12645811.fastq.gz	Fastqsanger.gz
	SRR12645714.fastq.gz	Fastqsanger.gz

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Single-cell RNA-sequencing of bleomycin-injured young and old mice

Project description:Young and old mice were first injected with bleomycin. At day 0, day 4 and day 14, the lungs were harvested and digested, and Lin-Epcam+ cells were isolated with FACS, single-cell RNA-seq was performed with the FACS-sorted cells.

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Project description:Transcriptional profiling from young, old, healthy, or injured rat iliac arteries.

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Project description:Transcriptional profiling from young, old, healthy, or injured rat iliac arteries. We studied the gene expression profile in a model of mechanical vascular injury in the iliac artery of aging (22 months old) and young rats (4 months old). We investigated aging-related variations in gene expression at 30 min, 3d and 7d post injury.

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Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Old mice showed delayed and incomplete lung function recovery 8 weeks after Bleomycin instillation. This shift in structural and functional repair in old Bleomycin-treated mice was reflected in a temporal shift in gene and protein expression. We reveal gene signatures and signaling pathways which underpin the lung repair process.

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Project description:The most preclinical used in vivo model to study lung fibrosis is the bleomycin-induced lung fibrosis model in 2-3-month-old mice. Although this model resembles key aspects of idiopathic pulmonary fibrosis (IPF), there are limitations in its predictability for the human disease. One of the main differences is the juvenile age of animals that are usually used in experiments, resembling humans of around 20 years. Because IPF patients are usually older than 60 years, aging appears to play an important role in the pathogenesis of lung fibrosis. Therefore, we here compared young (3 months) and old mice (21 months) 21 days after intratracheal bleomycin instillation. Analyzing lung transcriptomics (mRNAs & miRNAs) and proteomics, we found most pathways to be similarly regulated in young and old mice. However, old mice show an imbalanced protein homeostasis as well as an increased inflammatory state in the fibrotic phase compared to young mice. Comparisons with published human transcriptomic data sets (GSE47460, GSE32537 and GSE24206) revealed that the gene signature of old animals correlates significantly better with IPF patients as well as it turned human healthy individuals better into “IPF patients” using an approach termed predictive disease modelling. Comprising, young and old animals show similarly molecular hallmarks of IPF. Additionally, old mice resemble several features associated with IPF more closely compared to young animals.

2023-01-05 | GSE173523 | GEO

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